Evidence map›Paper›PMID 25886856›Full record

Observational studyCritical care (London, England)2015

Copeptin levels are associated with organ dysfunction and death in the intensive care unit after out-of-hospital cardiac arrest.

Giuseppe Ristagno, Roberto Latini, Mario Plebani, Martina Zaninotto, Jukka Vaahersalo, Serge Masson, Marjaana Tiainen, Jouni Kurola, Flavio Gaspari, Valentina Milani and 3 more

Abstract readObservational Study
In one paragraph

Observational study in Critical care (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Trial
  2. Biomarker patterns in patients with cardiogenic shock versus septic shock.International journal of cardiology. Heart & vasculature · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Giuseppe RistagnoDepartment of Cardiovascular Research, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Via La Masa, 19 - 20156 Milano, Milan, Italy. gristag@gmail.com.
Roberto LatiniDepartment of Cardiovascular Research, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Via La Masa, 19 - 20156 Milano, Milan, Italy. roberto.latini@marionegri.it.
Mario PlebaniDepartment of Laboratory Medicine, University-Hospital of Padova, Via Giustiniani 2, 35128, Padova, Italy. mario.plebani@unipd.it.
Martina ZaninottoDepartment of Laboratory Medicine, University-Hospital of Padova, Via Giustiniani 2, 35128, Padova, Italy. martina.zaninotto@sanita.padova.it.
Jukka VaahersaloDivision of Intensive Care Medicine, Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Haartmaninkatu 4, 00290, Helsinki, Finland. jukka.vaahersalo@hus.fi.
Serge MassonDepartment of Cardiovascular Research, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Via La Masa, 19 - 20156 Milano, Milan, Italy. serge.masson@marionegri.it.
Marjaana TiainenDepartment of Neurology, Helsinki University Hospital, Haartmaninkatu 4, 00290, Helsinki, Finland. marjaana.tiainen@hus.fi.
Jouni KurolaCentre for Prehospital Emergency Care, Kuopio University Hospital, P.O. Box 100, FI 70029, Kuopio, Finland. jouni.kurola@kuh.fi.
Flavio GaspariLaboratory of Pharmacokinetics and Clinical Chemistry, IRCCS-Istituto di Ricerche Farmacologiche 'Mario Negri', Villa Camozzi, 24020, Ranica, Italy. flavio.gaspari@marionegri.it.
Valentina MilaniDepartment of Cardiovascular Research, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Via La Masa, 19 - 20156 Milano, Milan, Italy. valentina.milani@marionegri.it.
Ville PettiläDivision of Intensive Care Medicine, Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Haartmaninkatu 4, 00290, Helsinki, Finland. ville.pettila@hus.fi.
Markus Benedikt SkrifvarsDivision of Intensive Care Medicine, Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Haartmaninkatu 4, 00290, Helsinki, Finland. markus.skrifvars@hus.fi.
FINNRESUSCI Study Group

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionWe studied associations of the stress hormones copeptin and cortisol with outcome and organ dysfunction after out-of-hospital cardiac arrest (OHCA).

methodsPlasma was obtained after consent from next of kin in the FINNRESUSCI study conducted in 21 Finnish intensive care units (ICUs) between 2010 and 2011. We measured plasma copeptin (pmol/L) and free cortisol (nmol/L) on ICU admission (245 patients) and at 48 hours (additional 33 patients). Organ dysfunction was categorised with 24-hour Sequential Organ Failure Assessment (SOFA) scores. Twelve-month neurological outcome (available in 276 patients) was classified with cerebral performance categories (CPC) and dichotomised into good (CPC 1 or 2) or poor (CPC 3 to 5). Data are presented as medians and interquartile ranges (IQRs). A Mann-Whitney U test, multiple linear and logistic regression tests with odds ratios (ORs) 95% confidence intervals (CIs) and beta (B) values, repeated measure analysis of variance, and receiver operating characteristic curves with area under the curve (AUC) were performed.

resultsPatients with a poor 12-month outcome had higher levels of admission copeptin (89, IQR 41 to 193 versus 51, IQR 29 to 111 pmol/L, P = 0.0014) and cortisol (728, IQR 522 to 1,017 versus 576, IQR 355 to 850 nmol/L, P = 0.0013). Copeptin levels fell between admission and 48 hours (P <0.001), independently of outcome (P = 0.847). Cortisol levels did not change between admission and 48 hours (P = 0.313), independently of outcome (P = 0.221). The AUC for predicting long-term outcome was weak for copeptin (0.62, 95% CI 0.55 to 0.69) and cortisol (0.62, 95% CI 0.54 to 0.69). With logistic regression, admission copeptin (standard deviation (SD) increase OR 1.4, 95% CI 1.03 to 1.98) and cortisol (SD increase OR 1.5, 95% CI 1.1 to 2.0) predicted ICU mortality but not 12-month outcome. Admission factors correlating with SOFA were shockable rhythm (B -1.3, 95% CI -2.2 to -0.5), adrenaline use (B 1.1, 95% CI 0.2 to 2.0), therapeutic hypothermia (B 1.3 95% CI 0.4-2.2), and copeptin (B 0.04, 95% CI 0.02 to 0.07).

conclusionsAdmission copeptin and free cortisol were not of prognostic value regarding 12-month neurological outcome after OHCA. Higher admission copeptin and cortisol were associated with ICU death, and copeptin predicted subsequent organ dysfunction.

Indexed as

Hospital MortalityAgedBiomarkersFemaleGlycopeptidesHumansHydrocortisoneHypothermia, InducedIntensive Care UnitsMaleMiddle AgedOrgan Dysfunction ScoresOut-of-Hospital Cardiac ArrestPrognosisProspective StudiesTreatment OutcomeBiomarkerscopeptinsGlycopeptidesHydrocortisone

Identifiers

PMID25886856
PMCPMC4415235

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.